Effects of hypoxic/anoxic brain injury

The effects of hypoxic or anoxic brain injury, where the brain is starved of oxygen, can range from mild, short-term symptoms such as dizziness or concentration problems, through to severe, long-term issues including vision, speech and memory.

Initial effects of anoxic brain injury

The body will respond to cerebral anoxia by increasing blood flow to the brain in an attempt to restore an adequate supply of oxygen. However, it is only possible to increase brain blood flow to about twice the normal level. If this is not enough to compensate for the anoxia, brain function will be disturbed and symptoms will become apparent.

If the cerebral anoxia is mild, there will be problems with concentration, attention, co-ordination and short-term memory, which may be relatively subtle to begin with. There may be headache, light-headedness, dizziness, an increase in breathing rate and sweating. There can be a restriction in the field of vision, a sensation of numbness or tingling and feelings of euphoria.

As the degree of anoxia becomes more pronounced, confusion, agitation or drowsiness appear, along with cyanosis - a bluish tinge to the skin, reflecting the lowered oxygen content of the blood, often most apparent around the lips, mouth and fingertips. There may be brief jerks of the limbs (myoclonus) and seizures, both resulting from the damaging effects of lack of oxygen on the brain. If the anoxia is severe, it will result in loss of consciousness and coma.

Because of their high demand for energy, the nerve cells of the brain are particularly sensitive to lack of oxygen. Although anoxia may produce damage to cells throughout the brain, some areas are more vulnerable than others. The cerebral cortex (especially the parietal lobes and occipital lobes), the hippocampus (important in memory), the basal ganglia and the cerebellum (both contributing to the control of movement) are particularly sensitive to anoxia.

When there is also an interruption of blood flow, as after a cardiac arrest, this may lead to damage in the areas furthest away from the territories supplied by the three major arteries of the brain. These 'watershed areas' are particularly vulnerable when blood flow is reduced and may suffer death of tissue (infarction), like that occurring in a stroke.

Severe anoxic brain injury may occasionally cause damage to the hypothalamus and pituitary gland, which are small structures at the base of the brain responsible for regulating the body's hormones. Damage to these areas can lead to insufficient or increased release of one or more hormones, which causes disruption of the body's ability to maintain a stable internal environment (homeostasis). In the early stages this can cause a condition called neurogenic diabetes insipidus, which is characterised by increased thirst and excessive production of dilute urine. This is due to a reduction in secretion of a hormone called vasopressin (anti-diuretic hormone) and can be treated by administering desmopressin (manufactured anti-diuretic hormone) and replacing lost fluids.

Cerebral anoxia may also produce brain swelling and this can add to the damage, by squeezing off smaller blood vessels and interrupting the local blood supply.

If there has been very severe anoxic damage to the brain, there may be a transition from coma into a persistent vegetative state (PVS). In PVS the basic brain functions of breathing spontaneously, maintaining the heartbeat and blood pressure, digesting food and producing urine all continue. However, even though there may still be a cycle of sleeping and waking and the eyes may open spontaneously, there is no real evidence of consciousness in any meaningful sense and no response to what is going on in the environment.

More recently, the possibility of a minimally conscious state has been recognised. This is distinct from PVS, because although it is still a state of profoundly altered consciousness, there is minimal but definite evidence of some limited self-awareness or awareness of the surroundings.

Severe anoxic brain injury is often fatal. In cases where the injury is so severe that there is no chance of recovery doctors may put in place orders that the patient is not resuscitated in the event of further complications, such as cardiac arrest.

Long-term effects of anoxic brain injury

The long-term consequences will depend on the severity of the cerebral anoxia and on how much irreversible damage has occurred in the brain. If there has only been mild or short-lived anoxia, there may well be recovery back to a normal or near normal level of functioning.

However, if the anoxic injury has been more marked the outcome is less certain and there are likely to be long-term effects. The nature of these problems will vary from person to person, depending on the severity of the injury and the brain areas affected.

There is considerable overlap with the effects of other kinds of acquired brain injury. However, the selective vulnerability of particular regions of the brain to anoxia also gives some distinctive features to this type of injury. A wide range of difficulties can occur, although not all are necessarily seen in every individual:

Damage to the cerebral cortex, the cerebellum and the basal ganglia may lead to limb weakness and disturbances of movement, balance and co-ordination. There may be spasticity or rigidity, with increased muscle tone. Anoxic injury to the basal ganglia may lead to abnormal movements, including tremor, involuntary writhing movements (athetosis) and brief, jerky movements (chorea).

The occipital lobe at the back of the brain contains the main visual centres and it is particularly susceptible to anoxia, which may cause a loss of visual function referred to as cortical blindness. Damage to the occipital lobe may also lead to conditions such as Anton'ssyndrome. This is a rare condition, in which a patient with cortical blindness may show no awareness of the loss of vision and deny any problem, despite walking into things and showing obvious evidence of an inability to see normally. Conversely, patients may experience blindsight, in which they may respond to visual stimuli without being consciously aware of being able to see.

The hippocampus, on the inner surface of the temporal lobe, is an important structure for memory function and it is sensitive to anoxic injury. Memory problems are very common following cerebral anoxia and they may be quite severe.

Disturbances of speech and language function may occur because of damage to areas of the brain involved in the production and articulation of speech, finding the right words and understanding language. Spoken and written communication may both be affected.

Damage to the frontal lobes may lead to disturbances in executive function - the ability to think and reason, to synthesize and integrate complex information and make considered judgements and decisions about what to do in a particular situation. These skills underlie the ability to plan for the future in a sensible way, as well as to function effectively in work and social settings.

Frontal lobe injury may produce changes in personality, including irritability, poor tolerance of frustration, impulsiveness and impairments in social perception and conduct. There may be apathy and lack of insight, as well as intermittent agitation and mood swings, or more sustained periods of depression. These changes may slow the progress of rehabilitation and make it difficult to achieve a successful return home.

Occasionally, severe anoxic injury can cause damage to the hypothalamus or pituitary gland, which can lead to a variety of hormonal problems, such as hypopituitarism. This is caused by a reduction in the release of hormones by the pituitary gland and symptoms include excessive tiredness, muscle weakness, decreased sex drive, inability to regulate body temperature, weight gain, low blood pressure, dry skin and headaches. Hormone replacement therapy can be used to treat hypopituitarism and other related disorders.

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